DAPK pairs of IFN γ inhibit PGCl3 malignant phenotype of.docVIP

 PAGE \* MERGEFORMAT 13 DAPK pairs of IFN γ inhibit PGCl3 malignant phenotype of 【Abstract】 Objective To investigate the tumor metastasis suppressor gene DAPK inhibition of IFN  γ highly metastatic lung cancer cell lines PGCl3 movement, invasion, adhesion, colony forming rate. Methods Liposome-mediated gene transfer method, using the eukaryotic plasmid expression vector pcDNA3.1, the tumor suppressor gene DAPK into highly metastatic lung cancer PGCl3 cells by G418 selection to obtain stable expression of the cell clones. DAPK observed PGCl3 enhanced INF  γ inhibit cell proliferation, movement, invasion, adhesion, colony forming efficiency. Results DAPK gene transfected PGCl3 cells INF  γ-sensitive. IFN  γ inhibited transfected DAPK gene PGCl3 cell proliferation, invasion capacity, exercise capacity, adhesion ability, clone formation rate, and the impact of IFN  γ dose-dependent manner. Conclusion tumor metastasis suppressor gene DAPK increased INF  γ inhibit PGCl3 cell malignant phenotype. Keywords: metastasis of lung cancer death-associated protein kinase 0 Introduction Death-associated protein kinase (death associated protein kinase, DAPK) is a new class of calcium / calmodulin-dependent kinase substrate protein to serine / threonine residues phosphorylated, the kinase was originally developed as interferon-γ (IFN  γ)-induced apoptosis as a positive regulator son was isolation and identification [1]. Studies have shown that many tumor cells is the inactivation of DAPK, the over-expression of DAPK inhibit cell proliferation and induce apoptosis, DAPK is a potential tumor suppressor genes and genes that inhibit tumor metastasis [2  4]. In this study, DAPK gene into highly metastatic human lung cancer cell lines (PGCl3 cell line), observed IFN  γ over-expression of DAPK on cell biology of lung cancer behavior. 1 Materials and methods 1.1 Materials PGCl3 cell line (Guangdong Medical biochemistry tea